ArticleJournal of immunology (Baltimore, Md. : 1950)2010
TIM-3: a novel regulatory molecule of alloimmune activation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- Enhanced suppressor function of TIM-3+ FoxP3+ regulatory T cells.European journal of immunology · 2014Trial
- Unlocking the Microbial Symphony: The Interplay of Human Microbiota in Cancer Immunotherapy Response.Cancers · 2025Review
- Moxibustion Regulates the Expression of T Cells in Rheumatoid Arthritis Through Tim-3/Gal-9 Signaling Pathway.Rejuvenation research · 2025Article
- Involvement of Tim-3 in Maternal-fetal Tolerance: A Review of Current Understanding.International journal of biological sciences · 2025Review
- Galectin-9: diverse roles in skin disease.Frontiers in allergy · 2025Review
- Inhibition of the TIM-1 and -3 signaling pathway ameliorates disease in a murine model of rheumatoid arthritis.Clinical and experimental immunology · 2024Article
- Regulatory T cells in lung disease and transplantation.Bioscience reports · 2023Review
- Immune Checkpoints in Solid Organ Transplantation.Biology · 2023Review
- Recombinant human TIM-3 ectodomain expressed in bacteria and recovered from inclusion bodies as a stable and active molecule.Frontiers in bioengineering and biotechnology · 2023Article
- Combinatorial Herpes Simplex Vaccine Strategies: From Bedside to Bench and Back.Frontiers in immunology · 2022Review
- Overexpression of PD-1 on T cells promotes tolerance in cardiac transplantation via ICOS-dependent mechanisms.JCI insight · 2021Article
- Evaluating Markers of Immune Tolerance and Angiogenesis in Maternal Blood for an Association with Risk of Pregnancy Loss.Journal of clinical medicine · 2021Article
- Recent Advances in Costimulatory Blockade to Induce Immune Tolerance in Liver Transplantation.Frontiers in immunology · 2021Review
- Serum Levels of T Cell Immunoglobulin and Mucin-Domain Containing Molecule 3 in Patients with Systemic Lupus Erythematosus.Journal of clinical medicine · 2020Article
- Galectin-9 is required for endometrial regenerative cells to induce long-term cardiac allograft survival in mice.Stem cell research & therapy · 2020Article
- Targeting novel inhibitory receptors in cancer immunotherapy.Seminars in immunology · 2020Review
- Development and validation of the immune signature to predict distant metastasis in patients with nasopharyngeal carcinoma.Journal for immunotherapy of cancer · 2020Article
- The Role of TIM-3 in Hepatocellular Carcinoma: A Promising Target for Immunotherapy?Frontiers in oncology · 2020Review
- TIM-3 as a Target for Cancer Immunotherapy and Mechanisms of Action.International journal of molecular sciences · 2017Review
- Advances in targeting co-inhibitory and co-stimulatory pathways in transplantation settings: the Yin to the Yang of cancer immunotherapy.Immunological reviews · 2017Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 3 countries.
Funding
Abstract
T cell Ig domain and mucin domain (TIM)-3 has previously been established as a central regulator of Th1 responses and immune tolerance. In this study, we examined its functions in allograft rejection in a murine model of vascularized cardiac transplantation. TIM-3 was constitutively expressed on dendritic cells and natural regulatory T cells (Tregs) but only detected on CD4(+)FoxP3(-) and CD8(+) T cells in acutely rejecting graft recipients. A blocking anti-TIM-3 mAb accelerated allograft rejection only in the presence of host CD4(+) T cells. Accelerated rejection was accompanied by increased frequencies of alloreactive IFN-γ-, IL-6-, and IL-17-producing splenocytes, enhanced CD8(+) cytotoxicity against alloantigen, increased alloantibody production, and a decline in peripheral and intragraft Treg/effector T cell ratio. Enhanced IL-6 production by CD4(+) T cells after TIM-3 blockade plays a central role in acceleration of rejection. Using an established alloreactivity TCR transgenic model, blockade of TIM-3 increased allospecific effector T cells, enhanced Th1 and Th17 polarization, and resulted in a decreased frequency of overall number of allospecific Tregs. The latter is due to inhibition in induction of adaptive Tregs rather than prevention of expansion of allospecific natural Tregs. In vitro, targeting TIM-3 did not inhibit nTreg-mediated suppression of Th1 alloreactive cells but increased IL-17 production by effector T cells. In summary, TIM-3 is a key regulatory molecule of alloimmunity through its ability to broadly modulate CD4(+) T cell differentiation, thus recalibrating the effector and regulatory arms of the alloimmune response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.